Translation elongation factor EF-P drives susceptibility to fluoroquinolone antibiotics in Bacillus subtilis
The emergence of antimicrobial resistance restricts the clinical efficacy of therapeutic antibiotic drugs. Elucidating the molecular mechanisms by which bacteria evade antibiotic activities will lead to novel therapeutic approaches. Therefore, it is critical to understand the mechanisms that govern susceptibility to antibiotics. Fluoroquinolones are a class of antibiotics widely used to treat…
The rise of antibiotic resistance hampers the effectiveness of therapeutic antibiotics. Investigating the molecular mechanisms behind bacterial resistance to antibiotics is crucial for developing novel treatment strategies. Fluoroquinolones, a class of antibiotics commonly used to treat infections caused by both Gram-positive and Gram-negative bacteria, have become less effective due to widespread resistance.
This resistance is primarily caused by point mutations in the genes encoding type-II topoisomerases, which are the cellular targets of fluoroquinolones. However, recent studies have also shown that alterations in translation can influence the fitness of bacteria during exposure to fluoroquinolones. Insertions in the gene encoding elongation factor P (EF-P) have been linked to increased survival against fluoroquinolones.
To better understand the role of EF-P in fluoroquinolone resistance, the researchers focused on the Gram-positive model organism Bacillus subtilis. They discovered that the absence of EF-P significantly enhances the survival of B. subtilis exposed to fluoroquinolones. Additionally, they found that the sensitivity to fluoroquinolones depends on the post-translational modification of EF-P, indicating that EF-P's activity plays a crucial role in its resistance function.
Interestingly, loss of EF-P also increases the survival of B. subtilis strains lacking RecA, a critical DNA repair protein necessary for the survival of fluoroquinolone drugs. By analyzing gene expression patterns, the researchers identified several key cellular response pathways that are differently regulated in EF-P-deficient cells during fluoroquinolone treatment.
Their findings suggest that EF-P regulates multiple mechanisms that contribute to the susceptibility of bacteria to fluoroquinolones.
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